Cadmium and zinc levels in the hair of smokers and nonsmokers
Transcript of Cadmium and zinc levels in the hair of smokers and nonsmokers
Portland State University Portland State University
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Dissertations and Theses Dissertations and Theses
7-31-1981
Cadmium and Zinc Levels in the Hair of Smokers Cadmium and Zinc Levels in the Hair of Smokers
and Nonsmokers and Nonsmokers
Neal R. Simonsen Portland State University
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AN ABSTRACT OF THE THESIS OF Neal R Simonsen for the Master of Science
in Biology presented July 31, 1981.
Title: Cadmium and Zinc Levels in the Hair of Smokers and Nonsmokers.
APPROVED BY MEMBERS OF
Richard R. Petersen
William E. Morton
To determine the relationship of tobacco and marijuana smoking
to levels of cadmium and zinc manifested in hair samples, a study was
conducted at Portland State University using atomic.absorption
spectrophotometry. 97 adult student volunteers participated in the
main study.
Tobacco smokers had significantly higher hair cadmium concen
trations and marijuana smokers had significantly higher zinc
concentrations than nonsmokers, confirming tobacco smoking as a
significant source of cadmium and implicating marijuana as a signi
ficant source of zinc. Higher average concentrations of cadmium among
marijuana smokers and zinc among tobacco smokers were also observed
but lacked statistical significance. Since cadmium is a toxic metal
with a long biological half-life and a tendency to accumulate in
certain target organs, particularly the kidney, the effects of smoking
upon the level of long-t~rm cadmium intake may have important conse
quences for health. In addition, comparative studies of hair metal
levels neglecting to take smoking habits into account are suspect at
least insofar as cadmium and probably zinc are concerned.
Trends toward increasing cadmium with age and observations of
decreased cadmium among individuals with black hair and increased
cadmium among individuals doing soldering are in general agreement
2
with previous findings but the lack of significantly higher cadmium
levels for males than for females contradicts previous work on
Americans. Different proportions of smokers in the subject populations
may be involved in this disagreement.
Former smokers had cadmium and zinc concentrations that did not
exceed the average concentrations for nonsmokers, indicating that hair
cadmium and zinc levels reflect exposure or intake rather than cumula
tive body burden.
CADMIUM AND ZINC LEVELS IN THE HAIR OF
SMOKERS AND NONSMOKERS
by
Neal R Simonsen
A thesis submitted in partial fulfillment of the requirements for the degree of
MASTER OF SCIENCE in
BIOLOGY
Portland State University
1981
TO THE OFFICE OF GRADUATE STUDIES AND RESEARCH:
The members of the Committee approve the thesis of
Neal R Simonsen presented July 31, 1981.
Richard R. Petersen
William E. Morton
APPROVED:
aylor, Head,
ACKNOWLEDGEMENTS
To the members of my thesis committee, for combining their
expertise to aid and abet a project that didn't fall neatly into any
one individual's field •..
To Marilyn Petersen and Barbara Stewart, for sharing their
experience in questionnaire design and statistical analysis,
respectively •..
And to everyone who volunteered a piece of themselves to make
this study possible
Thanks.
ACKNOWLEDGEMENTS • •
LIST OF TABLES .
LIST OF FIGURES
LIST OF APPENDICES .
BACKGROUND . • .
INTRO DUCT ION .
MATERIALS AND METHODS
RESULTS .
DISCUSSION .
LITERATURE CITED
APPENDICES . . .
TABLE OF CONTENTS
. . . . . . . . . . . . . .
PAGE
iii
v
vi
vii
1
10
15
19
31
38
47
LIST OF TABLES
TABLE PAGE
I Comparison of Hair Cadmium Levels and Current Smoking
Habits--Pilot Study • . . . . • . . . . . . . . . . . 20
II Comparison of Hair Cadmium Levels and Current Smoking
Habits--Main Study . . . . . . . . . • • . . . • • . 21
III Comparison of Hair Zinc Levels and Current Smoking
Habits . . . . . . . . . . . . . . . . . . . . . . . 22
IV Comparison of Hair Cadmium Levels and Current Smoking
Habits--Alternate Grouping, Main Study • • . . . . . 24
V Comparison of Hair Cadmium and Zinc Levels for Current,
Former and Non-Smokers . . . . . . • . . .
VI Cadmium and Zinc Concentrations (µg/g) in Hair vs.
Age (years) .••..•..........
VII Differences in Hair Cadmium and Zinc Levels (µg/g)
Associated with Miscellaneous Factors •....
VIII Hair Cadmium Concentrations (µg/g) for Individuals,
IX
Grouped According to Smoking Habits
Hair Zinc Concentrations (µg/g) for Individuals,
Grouped According to Smoking Habits •..••
26
27
30
52
53
LIST OF FIGURES
FIGURE PAGE
1. Cadmium Concentration in Hair {µg/g) as a Function of
Age (years) for Male and Female Nonsmokers . • . . • . 28
2. Cadmium Concentration in Hair (µg/g) as a Function of
Body Weight (lbs) for Male and Female Nonsmokers . . • 29
APPENDIX
A.
B.
c.
D.
E.
LIST OF APPENDICES
Previous Studies on Cd and Zn in Human Hair .
Informed Consent and Sample Questionnaire ...
Hair Cadmium Concentrations (µg/g) for Individuals,
Grouped According to Smoking Habits .....
Hair Z1nc Concentrations {µg/g) for Individuals,
PAGE
48
49
52
Gro4ped According to Smoking Habits . . . . • • . 53
Surrnnary of Selected Questionnaire Responses--Main
Study . . . . . . . . . . . . . . . . . . . . 54
BACKGROUND
In 1817 Friedrich Strohmeyer isolated cadmium, a metallic element
with an abundance in the earth's crust of less than one part per
million. Although rare in nature, cadmium is usually closely associ
ated with zinc, another member of group IIB of the periodic table with
which it shares many properties. Unlike zinc, however, cadmium is
highly toxic, a fact which was recognized about a century ago and has
become more important as increasing refining of zinc and other metal
ores and the discovery of an increasing variety of uses for cadmium
has led to increased exposure to cadmium in the general as well as
th~ industrial environment (Fasset and Irish 1978). The potential
hazards of cadmium exposure to the general population began to draw
wider interest after the implication of cadmium in a debilitating
syndrome in Japan dubbed Itai-Itai or "ouch-ouch" in recognition of
the agony associated with its characteristic bone deformation (osteo
malacia) and greatly increased proneness to bone fracture. Consumption
of contaminated rice grown in cadmium-rich waste water from a mining
operation was cited as the primary cause for this disease (Flick et al.
1969; Nomiyama 1980). Since that time, much progress has been made in
the investigation of potential health hazards of acute and chronic
cadmium exposure.
The general effects of acute exposure to cadmium are well
established: renal damage and dysfunction, osteoporosis, enteropathy
and anemia, plus lung damage and dysfunction (i.e. pulmonary edema
and interstitial pneumonitis) if exposure is via inhalation (DHEW
1977; Friberg et al. 1974). The effects of chronic cadmium exposure
are likely to be of much more importance to both industrial workers
and the general population but are less well established. They may
be characterized both by specific effects on normal metabolic pathway
functions and more generalized health effects, as will be detailed.
Cadmium was tentatively linked to hypertension when Schroeder
and Vinton (1962) described the development of hypertension in rats
given small doses of cadmium in drinking water. Hypertension in
response to cadmium was substantiated by two later studies (Schroeder
1964a; Schroeder and Buckman 1967a). A potential role of cadmium
as a human hypertensive agent was indicated by Schroeder's (1964b)
analysis of autopsy data collected by Tipton and Cook (1963) which
indicated a presence of high cadmium-to-zinc ratios in cadavers of
hypertensive subjects. Direct vasoconstriction and increased cardiac
output were suggested as mechanisms for the induction of hypertension
by cadmium, based again on experiments with rats (Perry et al. 1967).
But in 1969 Morgan found no elevation of cadmium levels in kidneys
2
or livers of hypertensive subjects and in an epidemiological study
(Holden 1969) no increase in the incidence of hypertension was noted
for subjects industrially exposed to cadmium. A link between cadmium
and cardiovascular disease death rates in the general population was
reported by Carroll (1966) with a marked correlation between those
death rates and cadmium levels in the air of 28 U.S. cities, and rein
forced by Hickey, Schoff and Clelland (1967) with similar findings
for cadmium and vanadium levels in the air of 26 cities. This link
was weakened in 1971 when Hunt et al. found no association between
cadmium in dustfall and cardiovascular disease rate in 77 cities,
and criticized Carroll's study on the grounds that population density
correlated more strongly than cadmium level with the death rate. More
recently, cadmium in water supplies has been linked to coronary heart
disease rates (Bierenbaum 1975), and in turn this link too has been
disputed (Sharrett 1977). Animal experiments continue to demonstrate
the induction of hypertension by cadmium (Perry et al. 1973; Doyle
et al. 1975; Revis 1977; Perry et al. 1980), but the potential role
of cadmium in human cardiovascular disease remains unsubstantiated.
The relationship of cadmium to emphysema also is unclear.
Although a number of studies have found evidence for an association
between chronic cadmium exposure and emphysema (Bonnell 1955; Holden
1965; Lewis et al. 1969), other studies have found no evidence for
such an association (Suzuki et al. 1965; Lauwerys et al. 1974).
There is good experimental evidence for a teratogenic role of
cadmium (Ferm et al. 1969; Schroeder and Mitchener 1971; Chernoff
1973; Earl and Vish 1979) and mixed evidence for carcinogenic (Heath
1962; Gunn et al. 1963; Schroeder et al. 1964c; Gunn et al. 1967;
Shimkin et al. 1978) and mutagenic (Epstein et al. 1972; Sissoeff
et al. 1976; Mitra and Bernstein 1978) roles in animals, and some
epidemiological evidence for the involvement of cadmium in human
cancer (Potts 1965; Lemen et al. 1976). The importance of cadmium
for the general population in regard to birth defects, mutations and
cancer, however, remains to be established.
3
Cadmium has also been shown to alter the i01T1une response in
experimental animals, particularly inhibiting ~he cellular component
(Cook et al. 1975; Loose et al. 1977; Muller et al. 1979); whether
this effect has significance for human health is unknown.
4
Associations of cadmium with some other disease conditions are
more straightforward. Changes in renal function of chronically exposed
workers have been observed repeatedly since Friberg (1948) found renal
damage and proteinuria in workers exposed to cadmium dust. Studies
verifying the association of cadmium with renal tubule damage and
excretion of low molecular weight proteins (particularly B2 micro
globul ins) have been widespread (e.g. Clarkson and Kench 1956; Nogawa
1980). Effects of cadmium on bone structure have been found in a
number of studies upon chronically exposed workers and experimentally
exposed animals. These studies have been extensively reviewed by
Friberg et al. (1974) and Nomiyama (1980).
Cadmium metabolism is highly complex. The route of intake is
of crucial importance to the impact of cadmium on the body. Cadmium
retention is variable but potentially is of a very long-term nature
and interactions with other metals and associated systems are myriad
and marked (Prasad 1976).
Intraperitoneal and intravenous intake of cadmium are obviously
of little significance under most circumstances despite the very high
retention rates (over 90%) reported for these routes (Moore et al.
1973). Oral intake of cadmium generally results in absorption of
3-5% (Thomas 1980), although retention rate decreases with increasingly
large doses (Moore et al. 1973); retention rates of from 1.5% to 29%
5
~ave been observed in humans (Nomiyama 1980). Intake of cadmium via
inhalation, on the other hand, usually results in absorption of between
10% and 50% (Friberg et al. 1974). Retention of inhaled cadmium is
$reatly influenced by the size of particles or form of chemical in !
which cadmium is inhaled (Nomiyama 1980). Retention of orally ingested
cadmium is apparently not influenced by chemical form but is sensitive
to dietary and physiological factors, e.g. calcium, protein, Vitamin D
and zinc levels (Moore et al. 1973; Nomiyama 1980).
Experiments on animals suggest that cadmium, once absorbed,
has a half-life of from 200 days for mice (Durbin et al. 1957) to
2 years for squirrel monkeys (Nordberg et al. 1971), with a tendency
toward decreasing rates of decline with increasing time from exposure.
Mathematical models based on excretion studies with humans project
10 to 30 year half-lives for whole body cadmium (Friberg et al. 1974).
Recently, Travis and Haddock (1980) have suggested that the biological
half-life of cadmium is age-dependent, declining from around 34 years
at birth to 11 years at age 80 as a result of progressive renal change.
Regardless of the exact biological half-life, cadmium interacts
~idely with other metal systems. The best known of these interactions
involves zinc. Zinc is an essential mineral involved in many vital
functions (Underwood 1971; Ochiai 1977). Cadmium has been charac
terized as an antimetabolite of zinc due to the inverse effect it
exerts on such factors as growth, lymphocyte count and hemoglobin
levels compared to zinc (Petering et al. 197la). While cadmium seems
to block many of the actions of zinc, the reverse is also true: thus,
zinc has been shown to have a prophylactic effect against acute
cadmium toxicity (Gunn et al. 1968). Competition for protein binding
sites in mucosal cells and tissues and zinc metalloenzymes is the
accepted explanation for this behavior (Underwood 1979).
Cadmium also seems to strongly affect calcium metabolism. It
is not clear, however, whether cadmium affects calcium metabolism
directly or indirectly: inhibition of 1-25 dihydrocholecalciferol
synthesis (Feldman and Cousins 1973) or alkaline phosphatase activity
(Ribas-Ozonas 1971) could affect bone by blocking intestinal calcium
6
uptake or bone deposition, for example. Recent studies confirm a
decrease in alkaline phosphatase activity in vivo, apparently induced
by degeneration of renal cells containing alkaline phosphatase
(Peereboom-Stegeman et al. 1979) and indicate a reduction in calcium
binding.protein in the intestinal mucosa with dietary exposure to
cadmium (Fullmer et al. 1980), thus suggesting that cadmium interferes
with calcium metabolism at both the intestinal and the kidney level.
Cadmium may interfere with nerve transmission by binding to Ca+2
receptor sites and preventing Ca+2 influx from enhancing neurotrans
mitter release at the presynaptic nerve terminals (Griffiths 1980).
Cadmium appears to also affect copper metabolism by displacing
copper from sulfhydryl binding sites on metallothionein, which serves
as the major copper-binding protein of the duodenum and liver (Evans
et al. 1970), producing decreased plasma, liver and bone copper levels.
Cadmium also appears to compete for iron binding sites in the intes
tinal mucosa, thus bringing about iron-deficiency anemia, while iron
in turn produces amelioration of some effects of chronic cadmium
toxicity (Bremner 1974). Finally, selenium, like zinc, has a protec
tive effect against acute cadmium poisoning (Gunn et al. 1968).
One of the keys to the ultimate fate of cadmium in the body
is metallothionein, a protein of molecular weight 6,000 to 10,000.
Metallothionein appears to be important in zinc and copper storage
and regulation. Binding of cadmium to metallothionein, however, forms
an exceptionally stable complex and hence metallothionein combines
7
with cadmium preferentially over these metals (Ochiai 1977). Synthesis
of metallothionein by kidney, liver and spleen is induced by exposure
to cadmium {Cherian and Goyer 1978; Suzuki et al. 1981) and cadmium
thionein complex is stably sequestered after resorption from the
glomerular filtrate primarily in the kidney parenchyma {Nordberg 1978).
This is thought to be a detoxification mechanism. When levels of
cadmium in the cortex of the kidney reach 100 µg/g, however, renal
tubular dysfunction may occur, and irreversible renal failure is
associated with accumulations of 200 µg/g (Friberg et al. 1974;
Cherian and Goyer 1978).
In light of the potential adverse health effects of cadmium,
an understanding of the environmental sources of exposure to cadmium
is important. The most obvious--and to date the most investigated-
sources of cadmium exposure are industrial. In fact, nearly all
cadmium exposure is essentially industrial, since cadmium concen
trations characteristic of undisturbed nature are very low (except
in the rare cadmium sulfide-based mineral greenockite) and relatively
immobile, but mining, refining and manufacturing processes provide
greatly improved opportunities for accumulation by animals and plants
alike. Nevertheless, industrial settings offer potentially heavy
exposure through welding, soldering, electroplating, pigment
manufacturing, and other processes which may involve the use of
8
cadmium (Hunter 1969). Exposure to air or water-borne cadmium produced
as a by-product of the refining of metals, particularly zinc, may
affect the general population as well as industrial workers.
The most obvious source of cadmium exposure which is not directly
industrial is diet. For the most part measured levels of cadmium
in food are quite low--below 0.05 µg/g (Friberg et al. 1974).
Conspicuous exceptions are shellfish in general and oysters in partic
ular (.1-7.8 µg/g; Pringle et al. 1968), anchovies and tea (5.39 and
1.38-2.50 µg/g respectively; Schroeder et al. 1967b).
Levels of cadmium reported in drinking water vary greatly.
Although "unpolluted" water has cadmium concentrations of less than
1 µg/L (Friberg et al. 1974), the APHA (1976) reports concentrations
ranging from 0.4 to 60 µg/L in U.S. drinking water. Altogether, from
both indirect calculations and based on analysis of foodstuffs and
average consumption (Duggan and Corneliussen 1972) and direct studies
of fecal excretion (Tipton and Stewart 1970), it is estimated that
total intake of cadmium in areas free of serious pollution will
generally be in the range of 40-50 µg/day in the U.S. The World
Health Organization has proyisionally established tolerable weekly
intake of cadmium as 400-500 µg (57-71 µg/day) for a "standard 60 kg
man 11 (Chef te 1 et a 1 • 197 2 ) •
A less obvious non-industrial source of cadmium is tobacco
smoking. A 1969 study of 6 brands of cigarettes found that an average
pack of 20 cigarettes contained nearly 23 µg of cadmium with only
minor variation between brands (Nandi et al. 1969). Menden et al.
(1972) measured the cadmium concentrations in whole cigarettes and
in mainstream smoke. They found that of 1.56 to 1.96 µg of cadmium
per whole cigarette, 0.10 to 0.12 µg was in particulate form in the
fraction of smoke normally inhaled. Based on this data it can be
estimated that smoking one pack of cigarettes per day will contribute
at least 2 µg to daily cadmium intake. This is not a large contri
bution to average raw intake, but much higher retention is to be
expected because the cadmium is inhaled rather than taken orally.
The potential contribution to daily cadmium retention of tobacco
smoking is thus quite substantial, being estimated at 1 µg/day for
a pack-a-day smoker versus 2.25 µg/day average retention via food
(Friberg et al. 1974).
9
Studies confirming the potential contribution of tobacco smoking
to retained cadmium and hence body burden have been conducted on
cadavers and, on a small scale, in vivo. In an autopsy study Lewis
et al. (1972) found a total burden of 14.2 mg of cadmium for kidney,
liver and lung combined in smokers and 6.8 mg in nonsmokers. Oster
gaard (1978) reported that renal cadmium concentrations in autopsied
samples from cigarette smokers were nearly twice as high as in non
smokers. Finally, Ellis et al. (1979) determined cadmium levels in
the left kidney and liver of 20 male volunteers using partial body
neutron activation and found tobacco smokers to have nearly double
the levels of nonsmokers in both organs.
INTRODUCTION
A more convenient analytical technique for cadmium other than
autopsy or partial body neutron activation would be of obvious value
in the investigation of aspects of cadmium metabolism, such as its
relationship with smoking, for studies on living subjects. Blood
analysis is a fairly common technique for investigating metals, but
levels of cadmium in the blood are unfortunately low. The median
normal concentration of cadmium is about 0.6 ng/g (Ediger and Coleman
1973} yet there can be enormous fluctuation. Values of less than
.5 to 14.2 µg/100 ml have been reported for whole blood in a single
study (Kubota et al. 1968), for example. This fluctuation may derive
in part from cadmium's rapid turnover rate upon entering the blood
stream. For example~ Shaikh and Lucis (1972b) reported that cadmium
levels in the plasma of rats declined within 48 hours after subcuta
neous administration of 109cd to the lower limit of detection. The
other common technique for determining metal levels in vivo, urin
alysis, also involves low sample concentrations: excretion of cadmium
appears to be mainly via the intestinal tract (Shaikh and Lucis 1972a),
which accounts for the relatively low urinary levels of cadmium,
generally in the range of 1-2 µg/L (Friberg et al. 1974). A less
common analytical technique, however, potentially offers specimens
with higher normal metal levels and lower concentration transience than
either blood or urine analysis. This technique is hair analysis.
Initial interest in analysis of hair for trace metals was
primarily for forensic applications. However, Kopito et al. {1967)
reported good correlation between hair lead content and clinical
11
findings of lead poisoning in children, and recorrmended the use of
hair analysis as a simple screening procedure. The use of hair
analysis in medical and biological applications has since grown {Maugh
1978; Klevay 1978), while frustration over the inability to control
for intra-individual variations in the distribution of elements has
dulled interest in forensic applications to the point that one worker
was moved to subtitle a report evaluating the forensic analysis of I
hair the "Failure of a mission" (Cornelius 1973).
Hair is a cystine-rich keratinized tissue. The disulfide bonds
formed between cystine residues of the helically-coiled polypeptide
chains which make up the keratin molecule give it most of its stability
(Baden et al. 1973; Hopps 1977). Sulfur groups in general and
cystine's in particular are also preferred binding sites for 11 heavy 11
trace metals 1 ike cadmium (Ochiai 1977); thus the same chemical
characteristics which stabilize the keratin of hair result in its
having high concentrations of many metals. Another valuable charac
teristic of hair is that it provides a relatively nonperishable
specimen. And, as a constantly forming tissue, it potentially acts
as a continual monitor of metal levels over time. A lock of hair
thus avoids the transience problems associated with blood or urine
specimens, for example, by providing an average reading of levels
over a long time period.
x
12
The question of the extent to which metal levels in hair reflect
actual body metal burdens is debated (e.g. Prasad et al. 1963; Oleru
1975; Maugh 1978; Chittleborough 1980). A fundamental problem is
determining just what "body burden" indicators should be compared
to hair metal concentrations since concentrations found in the body
normally vary from tissue to tissue and hair may be considered a
tissue itself. Numerous studies have demonstrated associations between
increased or decreased intake, or tissue levels in general, and hair
levels, from which many investigators have concluded, as did Hopps
(1977), that hair ii suitable for evaluating body stores.
Schroeder and Nason (1969) apparently published the first survey
of cadmium concentrations in human hair. In a study of 117 males
and 47 females using atomic absorption spectrophotometry they found
average levels of 2.76 µg/g for men and 1.77 µg/g for women, with
lower levels of cadmium for older than for younger women. They also
studied zinc, and found essentially identical average levels of 167
and 172 µg/g for men and women, respectively, with no significant
difference with age. Another 1969 study, using spark source mass
spectrometry (Yurachek et al.), found cadmium concentrations in hair
ranging from 0.34 to 1.8 µg/g but apparently involved only a few
subjects; values of 143 to 246 µg/g were found for zinc. Values of
cadmium and zinc levels published in these and subsequent studies
are summarized in Appendix A.
Studies of hair cadmium directed to more specific purposes fol
lowed these initial works. Mean hair levels of cadmium, as well as
lead, accurately reflected community exposure in investigations by
Hammer et al. (1971), results which were mirrored by investigations
of cadmium, mercury and lead by Chattopadhyay et al. (1977). Zinc
levels did not reflect exposure and this was attributed to relatively
small differences in total zinc exposure between groups, due in part
to the large normal dietary zinc component, and the possession of
13
more effective homeostatic mechanisms for zinc than for cadmium. Eads
and Lambdin (1973) report a decline in cadmium and zinc in the hair
of females in the age range from 32 to 72 years and higher zinc levels
in darker colored hair for both sexes which, they concluded, impli
cated zinc in the production of melanin involved in hair pigmentation.
Oleru (1976) compared cadmium levels in kidney, liver, hair and lungs
for 50 autopsied New Yorkers and found significant positive correla
tions between all 4 tissues, with a particularly strong correlation
between kidney and hair (0.52). Oleru also reported a general increase
in hair and kidney cadmium levels with age. Finally, in experimental
studies on laboratory animals, Kollmer and Berg (1979) found the- amount
of cadmium detected in hair as well as total body, various tissues,
and blood samples to be proportional to doses of cadmium administered
intravenously.
Hair studies of only zinc had preceded those including only
cadmium or both elements. Bate and Dyer (1965), Perkons and Jervis
(1966), and Harrison et al. (1969) surveyed hair for zinc and other
metals. In 1966 Strain et al. found good correlations between low
zinc levels in hair and zinc deficiency syndromes. Petering et al.
(197lb} found a close relationship between decreasing hair zinc concen
tration and age for males over 15 and for females, with no significant
X.
difference in levels between the sexes. A study by Obrusnik et al.
(1973) revealed a slight decrease in concentration of zinc with
distance from the scalp, contrasting with a previous study (1972)
14
by the same group which had found no such decrease, but another study
(Rendic et al. 1976) found zinc concentrations essentially constant
along the length of hair from O to30cms distal. Experimental studies
by Deeming and Weber (1977) found good correlations between dietary
zinc intake and hair zinc levels in rats. Finally, McKenzie (1979)
reported no significant differences between hair zinc levels in oyster
openers or industrial workers and unexposed individuals with the
exception of galvanizers, but there was a significant difference
between levels in the sexes (195 µg/g for females vs 180 µg/g for
males).
Despite the discovery of substantial amounts of cadmium in
tobacco and its potential contribution to cadmium exposure when smoked,
no previous studies have examined the possible contribution of mari
juana smoking to cadmium exposure. Nor were there any studies
exploring the relationship between cadmium and zinc levels in human
smokers and nonsmokers or even the impact of smoking on hair metal
levels in evidence in the literature. Thus, this study investigates
the relationship of cadmium and zinc levels in hair to smoking habits,
including both tobacco and marijuana use.
MATERIALS AND METHODS
The research project entailed. two separate studies, an initial
small scale pilot study being carried o~t six months prior to the
main study. Particulars in which the pilot study differed from the
main study are indicated following the general descriptions.
Subjects and Sample Collection
Volunteer subjects were recruited from students enrolled in
biology courses at Portland State University. The volunteers completed
an informed consent form and a separate anonymous questionnaire (iden
tified only by a code number) covering tobacco and marijuana smoking
habits, and a variety of other factors which potentially affect hair
trace metal levels. The questionnaire is reprinted in Appendix B.
Hair samples were taken from the occipital region of the scalp
within 24 hours after the hair had last been washed and were stored
in clean plastic bags. Only the portion of the hair strand within
6 cm of the scalp was used in the subsequent analysis.
In the pilot study no restriction was placed on the distance
of analyzed hair sections from the scalp.
Laboratory Reagents and Cleansing Protocol
All chemicals used were of A.C.S. reagent grade. All distilled
water used was deionized by passage through an ion exchange column.
Stock standards for atomic absorption spectroscopy were prepared in the
lab by dissolving cadmium (Cd) and zinc (Zn) metal in acid; fresh
16
working standards were made prior to spectroscopic analysis of samples.
Standards were made in 0.4 M HN03 to minimize loss of cadmium from
solution through adsorption onto the container walls.
All glassware (pyrex) used in sample pretreatment and digestion
and plasticware (linear polyethylene) used in sample storage was
subjected to a stringent cleansing procedure entailing four major
steps, each step followed by rinsing with deionized distilled water.
These steps consisted of: 1) Washing and scrubbing with hot tap
water; 2) Soaking at least 12 hours in nonionic detergent solution
prepared with distilled water; 3) Soaking in 2 M HCl; and 4) Letting
stand for 2 hours filled with 3 M HN03•
Sample Pre-treatment
Samples of 0.2 to 0.6 gram of hair were placed in 50ml beakers
in which they were rinsed twice with distilled water and then, after
addition of about 35ml of distilled water, placed on a mechanical
agitator for 40 minutes. Following agitation the washwater was poured
off and the samples rinsed three times with distilled water and
placed in a drying oven at 110°C overnight. Samples were stored in
a desiccator after drying until ready for use. Duplicates were pre
pared for hair samples of one gram or more.
In the pilot study a 30 minute nonionic detergent wash was used
instead of the 40 minute water wash.
Sample Digestion and Analysis
Washed, dried hair samples of from 0.2 to 0.6 g were weighed
to ± 1/10 mg into 25ml Erlenmeyer flasks. After addition of 6ml
5:1 HN03:H2o samples were covered with watchglasses and allowed to
sit overnight. The flasks were then placed on hot plates where after
50 minutes of gentle heating they were cooled for 10 minutes, the
watchglasses were removed, 4ml of cone. HN03 was added, and heating
was continued for about 3 hours. At this point the s~mples were
allowed to cool for 15 minutes, 2ml of 1:2 HC104:HN03 was added and
gradual heating to a gentle boil (c. 110°C) continued for another
17
hour and 40 minutes, when they were again allowed to cool for 15
minutes and then transferred to lOml beakers. The samples were then
heated until a clear solution was obtained and just enough solution
remained to cover the bottom of the beakers, HN03 being added dropwise
whenever a solution darkened, and then allowed to cool. When cool,
samples were transferred to 5ml volumetric flasks and 1:20 HN03:H2o was added to bring the solutions to 5ml. These solutions were then
stored in 5ml polyethylene bottles prior to analysis.
Reagent blanks were treated with the same procedure for each
batch of hair samples.
Digested hair sample solutions and standards were analyzed for
Cd by direct aspiration into an IL 551 atomic absorption spectrophoto
meter in flame mode under standard conditions (as per IL 551 Operator's
Manual). Replicate determinations of Cd were made for each sample,
and the order in which the samples were analyzed was reversed for
the second determination. Accurate determination of Zn required
dilution of the original sample solution. Thus, remaining volume
permitting, samples were then diluted ten-fold by pipetting 1.00ml
of sample into a lOml volumetric flask, diluting to volume with
deionized water and transferring the diluted solution to a 20ml
polyethylene bottle. These solutions were then analyzed for Zn using
the same general methodology as for Cd.
In the pilot study hair samples were weighed out onto weighing
paper which was then folded into packets and samples were gradually
added to the digestion medium as digestion proceeded. No HC104 was
used in the pilot study, nor was the initial digestion carried out
in a 25ml Erlenmeyer. Instead all digestion was carried out in lOml
beakers, using HN03 exclusively.
18
RESULTS
The pilot study included a total of 37 subjects, all of whom
were tested for hair cadmium. Table I sunmarizes the data obtained
for cadmium levels in the hair of the group as a whole and of subdivi
sions based on sex and smoking habits. The main study included a
further 97 subjects, all of whom were tested for cadmium and 72 of
whom were tested for zinc. On the average, 40-45% of the individuals
in classes recruited volunteered in the main study. Concentrations
ranged from 0.28 to 3.58 µg/g for cadmium and from 99 to 300 µg/g
for zinc. Tables II and III summarize the data obtained for cadmium
and zinc, respectively. Individual values for cadmium and zinc by
smoking habits and sex are presented in Appendices C and D.
In both studies the average cadmium level in the hair of current
tobacco smokers (1.35 and 0.97 µg/g for the pilot and main study,
respectively) exceeded that of nonsmokers (0.69 and 0.71 µg/g for
pilot and main study). This difference was statistically significant
in both studies (P=.031 for main and .048 for pilot study). Since
Bartlett's Test for homogeneity of variance indicated that the cadmium
data summarized in Tables I and II deviated significantly from homo
geneity unless it was logarithmically transformed, an additional ANOVA
was performed on log transformed data. This analysiss toos yielded
statistically significant results for the main study (P=.036_) 9 but
results for the pilot study exceeded the limit of statistical signi
ficance after transformation (P=.080). In addition, the average
TABL
E I
COM
PARI
SON
OF H
AIR
CADM
IUM
LEVE
LS A
ND C
URRE
NT S
MOKI
NG H
ABIT
S--P
ILOT
STU
DY
(Val
ues
are
Con
cent
rati
ons
in µ
g/g:
x
±SE
(n
))a
1 C
urre
nt t
obac
co
smok
ers
2 C
urre
nt m
arij
uana
(b
ut
not
toba
cco)
sm
oker
s
3 N
ot c
urre
nt s
mok
ers
Sig
nif
ican
t in
ter-
row
b
diff
eren
ces
All
I. 35
± •
22
( 8)
0.85
± .
22
(8)
0.69
± .
14
(21)
0.86
(3
7)
1 vs
. 3
P=.0
48
(. 08
0)
Mal
es
I. 60
± •
28
( 5)
0.74
±
.44
(2)
0.64
± .
24
(7)
0.99
± .
17
(14)
1 vs
. 3
P=.0
21
(. 0
79)
a x
= a
vera
ge;
SE =
sta
ndar
d er
ror
of t
he m
ean;
n
= n
umbe
r of
sub
ject
s
b S
igni
fica
nce
leve
ls
in p
aren
thes
es a
re f
or
log
tran
sfor
med
dat
a
Fem
ales
0.94
±
.36
(3)
0.89
±
.25
(6)
0.72
±
.17
(14)
0.79
± .
13
(23)
Sig
nifi
cant
in
ter-
colu
mn
diff
eren
ces
N
0
....
....
....
....
.. ..
.._
__
__
__
... .
._ _
_ ..
... .
...o
w--
... .
....
....
....
....
....
.. --
....
....
.. _
..
....
... ---
....
....
. ---
....
. --
....
....
..
_ ..
....
....
....
....
....
....
....
.. .
..
TABL
E II
COM
PARI
SON
OF H
AIR
CADM
IUM
LEVE
LS A
ND C
URRE
NT S
MOK
ING
HABI
TS--M
AIN
STUD
Y (V
alue
s ar
e C
once
ntra
tion
s in
µg/
g:
x ±
SE
(n))
a
1 C
urre
nt t
obac
co s
mok
ers
2 C
urre
nt m
ariju
ana
(but
no
t to
bacc
o)
smok
ers
3 N
ot c
urre
nt s
mok
ers
Sig
nifi
cant
in
ter-
row
b
diff
eren
ces
All
0.97
±
.11
(16)
0. 7
8 ±
.1
3 ( 1
0)
0. 7
1 ±
• 0
5 ( 7
1)
0. 7
6 (9
7)
1 vs
. 3
P=.0
31
(. 0
36)
Mal
es
1.12
±
.15
(8}
0.83
±
.21
(4)
0.67
± .0
8 (3
0}
0.77
±
.06
(42)
1 vs
. 3
P=.0
18
(. 0
45)
ax
= a
vera
ge;
SE
= s
tand
ard
erro
r of
the
mea
n;
n =n
umbe
r of
sub
ject
s
b S
igni
fica
nce
lev
els
in p
aren
thes
es a
re f
or l
og t
rans
form
ed d
ata
Fem
ales
0.82
±
.15
(8)
0.75
±
.17
(6)
0.74
±
.07
(41)
0.75
±
.06
(55)
Sig
nifi
cant
in
ter-
colu
mn
diff
eren
ces
N ......
TABL
E II
I
COM
PARI
SON
OF H
AIR
ZINC
LEV
ELS
AND
CURR
ENT
SMOK
ING
HABI
TS
(Val
ues
are
Con
cent
rati
ons
in µ
g/g:
x
±
SE
(n))
a
All
M
ales
Fe
mal
es
1 C
urre
nt t
obac
co
smok
ers
204
±
15
(14)
19
5 ±
21
(7)
212
± 2
1 (7
)
2 C
urre
nt m
ariju
ana
(but
23
7 ±
32
(6
) 23
0 ±
32
(3)
245
± 3
2 (3
) no
t to
bacc
o)
smok
ers
3 N
ot c
urre
nt s
mok
ers
180
± 8
(52
) 16
4 ±
12
(2
2)
192
± 1
0 (3
0)
189
(72)
17
7 ±
10
(32)
19
9 ±
9
(40)
Sig
nifi
cant
2
vs.
3 in
ter-
row
P=
.019
di
ffer
ence
s
a x
=av
erag
e; S
E=
stan
dard
err
or o
f th
e m
ean;
n
=num
ber
of s
ubje
cts
Sig
nifi
cant
in
ter-
colu
mn
diff
eren
ces
P=.0
80
N
N
23
cadmium level observed for current marijuana smokers who were not
also current tobacco smokers (0.79 and 0.78 µg/g for pilot and main
study, respectively) exceeded that of nonsmokers but not significantly
so. These relationships held for the group as a whole and for each
sex individually. (Tables I and II)
Average hair zinc levels for current tobacco smokers (204 µg/g)
also exceeded those for nonsmokers (180 µg/g) but not significantly
so. However, average zinc levels for current marijuana-but-not
tobacco smokers (237 µg/g) did significantly exceed (P=.019) those
for nonsmokers and were also observed to exceed those for current
tobacco smokers. This relationship, too, held for the group as a
whole and for both sexes individually. (Table III)
In the pilot study, average cadmium levels for males exceeded
those for females but average levels for nonsmoking males were lower
than those for nonsmoking females; neither difference was, however,
significant. In the main study observed average cadmium levels for
males were essentially the same as those for females for both smokers
and nonsmokers. Zinc levels, on the other hand, appeared higher for
females than for males regardless of smoking habits (199 vs. 177 µg/g,
P=.080). (Table III)
An alternative analysis of the data on smoking habits and hair
cadmium concentration is surrmarized in Table IV. The average hair
Cd level observed for heavy (tobacco) smokers (1.06 µg/g) exceeded
that for nonsmokers (P=.014), as did the average level for light
(tobacco and/or marijuana) smokers (0.79 µg/g; P=.430). In addition,
TABL
E IV
COM
PARI
SON
OF H
AIR
CADM
IUM
LEVE
LS A
ND C
URRE
NT S
MOKI
NG S
TATU
S-
ALTE
RNAT
E GR
OUPI
NG,
MAIN
STU
DY
(Val
ues
are
Con
cent
ratio
ns i
n µg
/g:
x ±
SE
(n
))a
All
M
ales
Fe
mal
es
1 H
eavy
tob
acco
sm
oker
sb
1.06
± .
13
(10)
1.
40
± •
18
( 5)
0. 7
2 ±
• 18
( 5
)
2 L
ight
tob
acco
and
/or
0. 7
9 ±
.10
(1
6)
0.75
± .
16
-(7
) 0.
83 ±
.14
(9
) m
ariju
ana
smok
ersC
3 N
onsm
oker
s 0.
71
± •
05
( 71)
0
. 6 7
± •
08
( 30
) 0
.74
± .
06
(41)
Sig
nifi
cant
1
vs.
3 1
vs.
3 in
ter-
row
P=
.014
P=
.015
di
ffer
ence
s
ax
= a
vera
ge;
SE =
stan
dard
err
or o
f th
e m
ean;
n
=num
ber
of s
ubje
cts
b O
ver
i pa
ck p
er d
ay
c 1
/3 t
o i
pack
per
day
for
tob
acco
or
at l
east
4 d
ays
per
mon
th f
or m
ariju
ana
Sig
nifi
cant
in
ter-
colu
mn
diff
eren
ces
N
.i=:-
the average Cd level observed for heavy smokers exceeded that for
light smokers (P=.110).
A comparison of current and former tobacco smokers is presented
in Table V. Both average hair cadmium and average hair zinc were
lower but not significantly so for former tobacco smokers (0.61 and
161 µg/g) than for current tobacco smokers or for nonsmokers (0.73
and 183 µg/g).
The results for relationship between age and hair cadmium are
summarized in Table VI and Figure 1. Cadmium concentration tended
25
to increase with age, although for females the relationship was rela
tively inconsistent and broke down after age 30. Zinc concentration
showed no discernible correlation with age (see Table VI).
The relationship between body weight and hair cadmium concen
tration was also examined but no apparent correlation was found.
Figure 2 surrmarizes these data.
Possible correlation of hair color, soldering, recent flu and
oral contraceptive use with hair metal levels was examined using the
cadmium and zinc measurements and the questionnaire responses. The
results are sunrnarized in Table VII. Black hair had a marginally
significant elevation in zinc level (P=.050). Observed but not statis
tically significant associations were noted between black hair, recent
flu, and oral contraceptive use and lower than average Cd levels where
as soldering was associated with higher than average levels; recent
flu and oral contraceptive use were also associated with lower than
average zinc levels.
"":
TABLE V
COMPARISON OF HAIR CADMIUM AND ZINC LEVELS FOR CURRENT, FORMER AND NON-SftllKERS
(Values are Concentrations in ug/g: x ±SE (n)f
1 Current tobacco smokers
2 Former tobacco smokers
3 Not current tobacco or marijuana smokers
S gnificant nter-row
d fferences
1 Current tobacco smokers
2 Former tobacco smokers
3 Not current tobacco or marijuana smokers
S gnificant nter-row
d fferences
All
0.97 ± .11 (16)
0.61 ± .13 (11)
0.73 ± .06 (60)
0.76
1 vs. 2 P=.042 1 vs. 3 P=.059
(97)
204 ± 14 (14)
161 ± 20 (7)
183 ± 8 (45)
185 (66)
1 vs. 2 P=.09
Males
Cd
1.12 ± .16 (8)
0.53 ± .18 (6)
0.71 ± .09 (24)
o. 77 ± .07 (38)
Zn
195 ± 20 (7)
158 ± 27 (4)
165 ± 13 (18)
171 ± 10 (29)
a 1r = average; SE= standard error of the mean; n = number of subjects
Females
0.82 ± .16 (8)
0.70 ± .20 (5)
0.74 ± .07 (36)
0.75 ± .06 (49)
212 ± 20 (7)
166 ± 31 (3)
194 ± 10 (27)
195 ± 9 (37}
26
27
TABLE VI
CADMilJfl AND ZINC CONCENTRATIONS (~g/g) VS. AGE (years)
Males Females All All
Age Males Females Tob. Smok. Non Smok. Tob. Smok. Non Smok.
Cd
17-20 0.66(6)a 0.73(13) 1. 52 (1) 0.49(5) 1.38(1) 0.68(12)
21-25 0.68(15) . 71(18) .69(4) .68(11) .75(4) . 70(14)
26-30 .74(9) .83(14) - .74(9) .65(3) .88(11)
31-39 .79(5) .61(6) .52(1) .85(4) .33(1) .67(5)
40-49 .99(1) - - .99(1)
50+ - 1.02(2) - - .80(1) 1.25(1)
Zn
17-20 217(5) 193 (11) 300(1) 197(4) 242(1) 188(10)
21-25 182(11) 209(11) 161(4) 194(7) 215(3) 207(8)
26-30 158(7) 199(11) - 158(7) 230(3) 188(8)
31-39 173(4) 188(3) 184(1) 169(3) 115( 1) 224(2)
40-49 166(1) - - 166(1)
50+ - 234(2) - - 279(1) 190(1)
a Numbers in parentheses are n values for corresponding concentrations
28
N 1Males v v --I
lJ) . . v
" v v G
~ v v--
v v v v t v. vv v ~ v v v v v v 'I v u.
' ~
~6 21 26 31 36 41 46 51 66 ASE CYEARS)
(\I r Females A
ud A A
A ~
Q A Gl ~A A ::::> A AA. ~
!S AA A~ A A
~ ~ AA AA 6 A A
~ AA A (S)
AA
I • I I
~6 21 26 31 36 41 46 51 56 AGE CYEARS:>
Figure 1. Cadmium concentration in hair (µg/g) as a function of age (years) for male and female nonsmokers.
N 1 Males --
Lt) l
" CD (D :::> v v-
~ v G)
I I
~25 135
N Females
LI) . I
" CD
! v-
~ A
G)
tf5 95
v v
v
v
Vv v
v 'I i v v
v vv,vvv iv v v v v v v v
I I I I
145 155 165 175 185 195 205 215 WEJ:&HT CL8S)
/::,. /::,. A
A A
A At A AA AA
AA 6 A
A A A ll.
A A
Aa ll. A A ~ Q A ~
~
t 05 t t 5 1 25 t 35 1 45 1 55 \IEIQtT CUSS)
29
Figure 2. Cadmium concentration in hair (µg/g) as a function of body weight (lbs) for male and female nonsmokers.
30
TABLE VII
DIFFERENCES IN AVERAGE HAIR CADMIUM AND ZINC LEVELS (µg/g) ASSOCIATED WITH MISCELLANEOUS FACTORS
Factor
Black hair
Soldering
Oral contraceptives
Recent flu
Subjects
7 black-haired male smokers
17 male nonsmokers
5 solderers
92 non-solderers
X Cd (n) x Zn
.542 ± .15 (4) 200 ± 19
.777 ± .09 (14) 155 ± 10
P=.20(.18)a P=.05
.833 ± .19
.744 ± .05
P=.65(.52)
(Only 2 Zn values were obtained for solderers)
Note: solderers include 2 individuals with black hair and 1 with recent flu.
6 oral. contra. users
35 nonusers
.578 ± .13
.763± .05
P=.20(27)
(5) 163 ± 26
(25) 197 ± 12
P=.23
Note: all users/nonusers compared for Zn are nonsmokers
3 males w/rec. flu .465 ± .32
39 males w/o rec. flu .795 ± .09
P=. 33( .17)
(3) 139 ± 28
(29) 181 ± 9
P=.18
Note: Males w/recent flu include 1 solderer, 1 with black hair, and 1 curr. tab. and mar. smoker
a P value in parenthesis is for log transformed data
DISCUSSION
The results of this study indicate that current tobacco smoking
is associated with elevated hair cadmium levels compared to nonsmoking
(ANOVA, P=.031). This observed elevation in hair cadmium levels is
consistent with the observation of higher cadmium body burdens for
tobacco smokers after autopsy (Lewis et al. 1972; Ostergaard 1978)
and in vivo (Ellis et al. 1979) studies of cadmium load, and with
the significant cadmium content of tobacco (1.56-1.96 µg/cigarette;
Menden et al. 1972). These data support the hypothesis that intake
of cadmium through tobacco smoking is reflected by higher cadmium
levels in hair as well as higher total body cadmium burden.
Although elevation of mean hair cadmium concentration in current
marijuana smokers was observed in both the main and pilot studies
and for both sexes, the relationship was not statistically significant.
Thus, although the data is consistent with the hypothesis that mari
juana smoking, too, contributes to cadmium exposure, the results are
inconclusive.
The observation of a smaller elevation of concentrations of
cadmium in the hair of marijuana smokers than of tobacco smokers
relative to nonsmokers is, however, consistent with the idea that
a smoker's average total consumption of marijuana is likely to be
much lower than that of tobacco. This is prompted by differences
in styles of usage, price, ease of obtainment and frequency of circum
stances where use is unacceptable (due to legal and/or social
pressures), all of which would presumably favor consumption of lower
quantities of marijuana than tobacco. This idea is borne out by the
observation of higher average hair cadmium concentrations in current
heavy tobacco smokers (1.06 µg/g) than in marijuana-light tobacco
smokers pooled (0.79 µg/g), while the average for this pooled group
is essentially the same as that for current regular marijuana-but
not-tobacco smokers alone (0.78 µg/g), and is also higher than that
for nonsmokers (0.71 µg/g) but not significantly so. (Table IV)
32
The average hair cadmium values obtained in this study are lower
than those obtained by Schroeder (1969), Eads and Lambdin (1973),
Petering et al. (1973), and Chattopadhyay et al. (1977) for urban
adults. The subjects of the present study were, however, relatively
young (average age under 26 years) and included a relatively small
proportion of smokers, both factors which, as previous and ensuing
discussion indicates, lower average cadmium concentrations should
be associated with. This study's values are in general agreement
with the work of Yurachek et al. (1969), and the values of Chatto
padhyay et al. (1977) for adults in nonindustrial settings.
(Appendix A)
The elevation of hair zinc levels in· tobacco smokers was ini
tially somewhat surprising. The competition for binding sites on
proteins that is associated with the metabolic antagonism of cadmium
and zinc suggested that zinc levels and overall zinc-cadmium ratios
might be lower in smokers. However, zinc normally was present in
hair at concentrations approximately 200-fold that of cadmium. Thus,
indications of any simple displacement or replacerrent phenomenon
of zinc by cadmium would be obscured by variation in zinc levels.
Furthermore, it is known that cadmium and zinc tend to be found in
close association in nature and that zinc is an essential nutrient
for plants in general (Epstein 1972; Gauch 1972) and tobacco in
particular (Hoagland et al. 1936), so it would not be surprising if
tobacco contained substantial amounts of zinc as well as containing
cadmium. The results, then, indicate that tobacco smoking may be
33
a source of exposure to zinc as well as cadmium, but again lack
sufficient statistical significance (P=.16) to be conclusive.
On the other hand, the results for zinc levels in current mari
juana smokers and nonsmokers are statistically significant (P=.019)
in their indication of an association between marijuana smoking and
elevated hair zinc levels. The explanation for this result may be
generally the same as that cited in the case of tobacco smokers.
~tabolic alteration by some inhaled component of the smoking material
is another possibility, but there are no data pertaining to trace
metal constituents of marijuana smoke and its effects on metal meta
bolism.
The overall results of this study also reflect upon the useful
ness of hair analysis as an indicator of body metal burden. If tobacco
smoking does serve as a source of cadmium, as previous studies and
the elevation of hair cadmium associated with current tobacco smoking
habits observed in this study suggest, and if hair metal levels do
reflect body metal burden, then former tobacco smokers as well as
current smokers should show higher hair cadmium concentrations than
nonsmokers. In fact, former smokers do not show a higher average
hair cadmium concentration than nonsmokers. (Only two of the twelve
former heavy tobacco smokers showed levels above the average for
nonsmokers.) This suggests that hair cadmium levels reflect recent
exposure rather than total body burden.
34
Average cadmium (and zinc) levels observed for former heavy
tobacco smokers are actually lower than those observed for nonsmokers,
but are not significantly different statistically (P=.43 for males
and .48 for females for Cd., .52 and .21 for Zn). The possibility
of an increase in metallothionein activity in response to cadmium
exposure via tobacco smoking which carries over after smoking ceases,
resulting in more effective sequestration of cadmium in internal organs
at the expense of hair, is an interesting but purely speculative inter
pretation of these observations.
Since zinc is an essential metal for humans and has effective
homeostatic regulation (Underwood 1971), body burden of zinc is not
expected to increase significantly unless intake is substantially
elevated. Thus the appearance of elevated zinc levels in the hair
of tobacco smokers appears anomalous unless the hair is viewed as
serving in the role of an excretory pathway to some extent. This
suggests that in the case of zinc, too, hair may reflect exposure
(an increase in which, results in increased excretion) rather than
body burden.
Average cadmium levels were higher for all males than for all
females in the pilot study but were essentially the same for all
individuals of both sexes in the main study. Although this at first
appears inconsistent, it is notable that in the pilot study the
fraction of males and females who were current tobacco smokers was
5/14 and 3/23, respectively, whereas in the main study the fraction
was 8/42 and 8/55. Thus the proportion of male current tobacco
smokers decreased by almost half between the two studies while the
proportion of female current tobacco smokers remained virtually
unchanged. Also notable is the fact that observed average levels
for male nonsmokers were actually lower--though not statistically
so--than those for female nonsmokers in both studies. The results
35
of this study regarding difference in hair cadmium between the sexes
are more in agreement with Petering et al. (1973) than the classical
results compiled by Schroeder and Nason (1969) or those reported by
Eads and Lambdin (1973}. Part of the discrepancy may arise from the
smoking variable, e.g. the proportion of the general U.S. population
who smoke is around 40% for ages 15-50 (DHEW 1979) while the proportion
of this project's main study population who smoked was under 20%.
In addition, Schroeder and Nason's and/or Eads and Lambdin's study
population may have contained an abnormally high proportion of male
smokers--and in any case more U.S. males smoked relative to females
at the time of the Schroeder study.
Hair zinc levels were lower for males than for females. This
may indicate a characteristic sex difference, for although not statis
tically significant (P=.080) the average levels of 177 µg/g and
199 µg/g for males and females, respectively, are in excellent agree
ment with the work of McKenzie (1979), who found mean concentrations
of 180 for males and 195 for females in a group of New Zealand students
ranging from 18 to 27 years of age. Klevay (1970) also found
significantly higher hair levels in females than males, and it is
notable that the 4 other studies which have compared concentrations
for both sexes, while reporting no significant difference between
the sexes, all observed higher average concentrations in females than
in males (Reinhold et al. 1966; Schroeder and Nason 1969; Petering
et al. 1971b; Eads and Lambdin 1973; also see Appendix A).
The trend toward increasing cadmium with increasing age is also
in general agreement with previous studies such as Eads and Lambdin's
(1973) and Oleru's (1976). For the women, however, the not-very
marked increase in the under 30 year age range and the irregularity
36
of results for the post-30 year range contradicts Petering et al. 's
1973 study's findings of a steady increase up to a peak between ages
40 and 50 and, for the men, the general increase with age also contra
dicts that study's findings of a levelling off around age 20. The
larger sample size of the Petering study (95 males and 83 females)
and its much broader age distribution caution against acceptance of
this project's indications regarding age and male hair cadmium levels.
Although it seemed probable that a general increase in food
intake would also serve to increase cadmium intake and thereby increase
hair levels, the lack of apparent correlation between weight and hair
cadmium level does not support this hypothesis. Perhaps a more_ direct
estimate of food intake such as daily calorie intake or body fat test
would be more successful in th;-s regard.
Finally, the findings for the influence of miscellaneous factors
on hair metal level, although in most cases involving too few samples
to be of statistical significance, are nonetheless worthy of comnent.
The lower average cadmium concentration for black haired males is
in agreement with previous findings (Schroeder and Nason 1969); the
exact cause for this relationship is unknown.but apparently involves
a difference{s) in structural makeup related to hair pigmentation.
The significantly higher zinc concentration for black haired males
37
is likewise in agreement with previous findings (Eads and Lambdin
1973). The higher cadmium among individuals who solder is consistent
with the high cadmium content of most solder (Fasset and Irish 1978)
and the observation of elevated blood and urine cadmium concentrations
in solderers (Welinder et al. 1977). No previous studies dealing
with the effect of oral contraceptive use or recent flu on hair
cadmium and zinc are known. Thus the finding that both seem to
depress hair cadmium and zinc levels cannot be compared to any previous
findings and must await verification before being considered signifi
cant. Still, oral contraceptives are known to alter trace metal
metabolism, including lowering serum and plasma zinc concentrations
(Smith and Brown 1976). And it is not unreasonable that a bout of
flu might put a heavy demand on zinc since zinc is involved in the
irrmune system, thus resulting in a decrease of zinc levels in hair
formed during the course of illness, although this does not explain
the concurrent depression in cadmium level.
LITERATURE CITED
American Public Health Association. 1976. Standard methods for the examination of water and wastewater. 14th ed. American Public Health Association, Washington, D.C. 1193pp.
Baden, H.P., L. Goldsmith and B. Fleming. 1973. A comparative study of the physicochemical properties of human keratinized tissues. Biochim. et Biophys. Acta 322: 269-278.
Bate, L.C. and F. Dyer. 1965. Trace elements in human hair. Nucleonics 23: 74-80.
Bierenbaum, M., et al. 1975. Possible toxic factor in coronary heartdisease. Lancet 1: 1008-1010.
Bonnell, J.A. 1955. Emphysema and proteinuria in men casting cadmium alloys. Br. J. Ind. Med. 12: 181-191.
Bremner, I. 1974. Heavy metal toxicities. Q. Rev. Biophys. 7: 75-124.
Carroll, R.E. 1966. The relationship of cadmium in the air to cardiovascular disease death rates. JAMA 198: 267-269.
Chattopadhyay, A., T. Roberts and R. Jervis. 1977. Scalp hair as a monitor of community exposure to lead. Arch. Environ. Health 32: 226-236.
Cheftel, H., et al. 1972. Evaluation of certain food additives and the contaminants mercury, lead, and cadmium. World Health Organization, Tee. Rep. Ser. 505: 20-24, 32.
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Chernoff, N. 1973. Teratogenic effects of cadmium in rats. Teratology 8(1): 29-32.
Chittleborough, G. 1980. A chemist's view of the analysis of human hair for trace elements. Sci. Total Environ. 14: 53-75.
Clarkson, T.W. and J. Kench. 1956. Urinary excretion of amino acids by men absorbing heavy metals. Biochem. J. 62: 361-372.
Cook, J.A., E. Hoffman and N. Luzio. 1975. Influence of lead and cadmium on the susceptibility of rats to bacterial challenge. Proc. Soc. Exp. Biol. Med. 150: 741-747.
Cornelius, R. 1973. Neutron activation analysis of hair: failure of a mission. J. Radioanal. Chem. 15: 305-316.
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Pestic. Monit. J. 5: 331-343.
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Eads, E. and C. Lambdin. 1973. A survey of trace metals in human hair. Environ. Res. 6: 247-252.
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39
Ediger, R.D. and R. Coleman. 1973. Determination of cadmium in blood by a Delves cup technique. Atomic Absorp. Newsl. 12: 3-6.
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Epstein, E. 1972. Mineral nutrition of plants: principles and perspectives. John Wiley and Sons, New York. 412pp.
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Evans, G.W., P. Majors and W. Cornatzer. 1970. Mechanism for cadmium and zinc antagonism of copper metabolism. Biochem. Biophys. Res. Comm. 40: 1142-1148.
Fassett, D.W. 1972. Cadmium. In Lee, D.H.K. (Ed.). Metallic contaminants and human health. Academic Press, N.Y. Pp. 97-124.
--.........--~--and D. Irish (Eds.). 1978. Toxicology. Patty's industrial hygiene and toxicology, II. Interscience, N.Y. 2,481pp.
Feldman, S.L. and R. Cousins. 1973. Inhibition of 1,25-dihydroxycholecalciferol synthesis by cadmium in vitro. Fed. Proc. 32: 918.
40
Ferm, V.H., D. Hanlon and J. Urban. 1969. The permeability of the hamster placenta to radioactive cadmium. J. Embryol. Exp. Morph. 22(1): 107-113.
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, et al. 1974. Cadmium in the environment. CRC Press, --~C ...... le_v_e.land. 248pp.
Fullmer, C.S., T. Oku and R. Wasserman. 1980. Effect of cadmium administration on intestinal calcium absorption and vitamin D-dependent calcium-binding protein. Environ. Res. 22: 386-399.
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Gunn, S.A., T. Gould and W. Anderson. 1963. Cadmium-induced interstitial cell tumors in rats and mice and their prevention by zinc. J. Nat. Cancer Inst. 31: 745-753 •
~~~~~~~~~~~~~~~
. 1967. Specific response of mesenchymal tissue to cancerigenesis by cadmium. Arch. Path. 83: 493-499.
___ __,,.. _ __,,,____,__...,,.... __ - ____ • 1968. Specificity in protection against lethality and testicular toxicity from cadmium. Proc. Soc. Exp. Biol. Med. 128: 591-595.
Hanmer, D.I., et al. 1971. Hair trace metal levels and environmental exposure. Am. J. Epidemiol. 93: 84-92.
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Heath, J.C., et al. 1962. Cadmium as a carcinogen. Nature 193: 592-593.
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Hoagland, D.R., W. Chandler and P. Hibbard. 1936. Little-leaf or rosette of fruit trees V. Effect of zinc on the growth of plants of various types in controlled soil and water culture experiments. Proc. Amer. Soc. Hort. Sci. 33: 131-141.
Holden, H. 1965. Cadmium fume. Ann. Occup. Hyg. 8: 51-54 .
• 1969. Cadmium toxicology. Lancet 2: 57. ----Hopps, H.C. 1977. The biologic bases for using hair and nail for
analyses of trace elements. Sci. Total Environ. 7: 71-89.
Hunt, W.F., et al. 1971. A study in trace element pollution of air in 77 midwestern cities. Trace Subst. in Environ. Health 4: 56-67.
Hunter, D. 1969. The diseases of occupations. 4th ed. Little, Brown and Co., Boston. 1259pp.
41
Hurshman, L.G., B. Brown and R. Guyton. 1978. The implications of sidestream cigarette smoke for cardiovascular health. J. Environ. Health 41: 145-149.
Klevay, L.M. 1970. Hair as a biopsy material I. assessment of zinc nutriture. Am. J. Clin. Nutr. 23: 284-289 .
. 1978. Hair as a biopsy material: progress and prospects. --...,,.A-rc...,.h-. Intern. Med. 138: 1127-1128.
Kollmer, W.E. and D. Berg. 1979. Interrelations between hair content, intravenous dose and retention of Cd in different rat-tissues. J. Radioanal. Chem. 52: 189-197.
Kopito, L., R. Byers and H. Shwachman. 1967. Lead in hair of children with chronic lead poisoning. New Eng. J. Med. 276: 949-953.
Kubota, J., V. Lazar and F. Losee. 1968. Copper, zinc, cadmium and lead in human blood from 19 locations in the United States. Arch. Environ. Health 16: 788-793.
Lauwerys, R.R., et al. 1974. Epidemiological survey of workers exposed to cadmium. Effect on lung, kidney and several biological indices. Arch. Environ. Health 28: 145-148.
Lemen, R.A., et al. 1976. Morality among workers exposed to cadmium. Ann. N.Y. Acad. Sci. 271: 273-279.
Lewis, G.P., H. Lyle and S. Miller. 1969. Association between elevated hepatic water-soluble protein-bound cadmium levels and chronic bronchitis and/or emphysema. Lancet 2: 1330-1333.
, et al. 1972. Cadmium accumulation in man: influence ---=---of smoking, occupation, alcoholic habit and disease. J. Chron. Dis. 25: 717-726.
Loose, L.D., J. Silkworth and D. Warrington. 1977. Cadmium-induced depression of the respiratory burst in mouse pulmonary alveolar macrophages, peritoneal macrophages and polymorphonuclear neutrophils. Biochem. Biophys. Res. Commun. 79: 326-332.
Maugh, T.H. 1978. Hair: a diagnostic tool to complement blood serum and urine. Sci. 202: 1271-1273.
McBean, L.D., et al. 1971. Correlation of zinc concentrations in human plasma and hair. Am. J. Clin. Nutr. 24: 506-509.
McKenzie, J.M. 1979. Content of zinc in serum, urine, hair, and toenails of New Zealand adults. Am. J. Clin. Nutr. 32: 570-579.
Menden, E.E., et al. 1972. Distribution of cadmium and nickel of tobacco during cigarette smoking. Environ. Sci. Technol. 6: 830-832.
Mitra, R.S. and I. Bernstein. 1978. Sin~le-strand breakage in DNA of Escherichia coli exposed to Cd2. J. Bacterial. 133: 75-80.
Moore, W., et al. 1973. Comparison of 115mcadmium retention in rats following different routes of administration. Environ. Res. 6: 473-478.
42
Morgan, J.M. 1969. Tissue cadmium concentration in man. Arch. Intern. Med. 123: 405-408.
MUller, S., et al. 1979. Effects of cadmium on the immune system of mice. Experientia 35: 909-910.
Nandi, M., et al. 1969. Cadmium content of cigarettes. Lancet 2: 1329-1330.
Nogawa, K., et al. 1980. Renal dysfunctions of inhabitants in a cadmium-polluted area. Environ. Res. 23: 13-23.
Nomiyama, K. 1980. Recent progress and perspectives in cadmium health effects studies. Sci. Total Environ. 14: 199-232.
Nordberg, G., L. Friberg and M. Piscator. In Friberg, L., M. Piscator and G. Nordberg. 1971. Cadmium in the environment. CRC Press, Cleveland. Pp. 30, 44.
Nordberg, G.F. and K. Nishiyama. 1972. Whole-body and hair retention of cadmium in mice. Arch. Environ. Health 24: 209-214.
Nordberg, M. 1978. Studies on metallothionein and cadmium. Environ. Res. 15: 381-404.
Obrusnik, I., et al. 1972. The variation of trace element concentrations in single human head hairs. J. Forensic Sci. 17: 426-439.
• 1973. The variation of trace element concen-~~~~~~~~
trations in single human head hairs. J. Radioanal. Chem. 15: 115-133.
Ochiai, E. 1977. Bioinorganic chemistry: an introduction. Allyn and Bacon, Boston. 515pp.
Oleru, U.G. 1975. Epidemiological implications of environmental cadmium I. the probable utility of human hair for occupational trace metal (cadmium) screening. Am. Ind. Hyg. Assoc. J. 36: 229-233.
____ • 1976. Kidney, liver, hair and lungs as indicators of cadmium absorption. Am. Ind. Hyg. Assoc. J. 37: 617-621.
43
Ostergaard, K. 1978. Renal cadmium concentration in relation to smoking habits and blood pressure. Acta Med. Scand. 203: 379-383.
Peereboom-Stegeman, J.H., et al. 1979. Influence of chronic Cd intoxication on the alkaline phosphatase activity of liver and kidney; biochemical, histochemical and histological investigations. Toxicol. 14: 67-80.
Perkons, A.K. and R. Jervis. 1966. Trace elements in human head hair. J. Forensic Sci. 11: 50-63.
Perry, H.M., et al. 1967. Mechanisms of the acute hypertensive effect of intra-arterial cadmium and mercury in anaesthetized rats. J. Lab. Clin. Med. 70: 963-972.
~~~~- and M. Erlanger. 1973. Elevated circulating renin activity in rats following doses of cadmium known to induce hypertension. J. Lab. Clin. Med. 82: 399-405.
----, et al. 1980. Inhibition of cadmium-induced hypertension in rats. Sci. Total Environ. 14: 153-166.
Petering, H.G., M. Johnson and K. Stemmer. 1971a. Studies of zinc metabolism in the rat I. dose-response effects of Cd. Arch. Environ. Health 23: 93-101.
, D. Yeager and S. Witherup. 197lb. Trace metal content __ __,,,...........__,........_
of hair I. zinc and copper content of human hair. Arch. Environ. Health 23: 202-207.
44
Petering, H.G., D. Yeager and S. Witherup. 1973. Trace metal content of hair II. cadmium and lead of human hair. Arch. Environ. Health 27: 327-330.
Potts, C.L. 1965. Cadmium proteinuria--the health of battery workers exposed to cadmium oxide. Ann. Occup. Hyg. 8: 55-61.
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~--~-(Ed.). 1976. Trace elements in human health and disease. II. Essential and toxic elements. Academic Press, N.Y. 525pp.
Pringle, B., et al. 1968. Trace metal accumulation by estuarine molluscs. J. Sanit. Eng. Div. Proc. Am. Soc. Civ. Eng. 94: 455-461.
Reinhold, J.G., et al. 1966. Zinc and copper concentrations in hair of Iranian villagers. Am. J. Clin. Nutr. 18: 294-300.
Rendic, D., et al. 1976. Trace-element concentrations in human hair measured by proton-induced X-ray emission. J. Invest. Dermatol. 66: 371-375.
Revis, N. 1977. A possible mechanism for cadmium-induced hypertension in rats. Life Sci. 22: 479-488.
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Schroeder, H.A. and W. Vinton. 1962. Hypertension induced in rats by small doses of cadmium. Am. J. Physiol. 202: 515-518 .
. 1964a. Cadmium hypertension in rats. Am. J. Physiol. ---..,...,,.-=-----.-..-207: 62-66 .
------• 1964b. Renal cadmium and essential hypertension. JAMA 187: 358.
------, J. Balassa and W. Vinton. 1964c. Chromium, lead, cadmium, nickel and titanium in mice: effect on mortality, tumors and tissue levels. J. Nutr. 83: 239-250.
------and J. Buckman. 1967a. Cadmium hypertension: its reversal in rats by a zinc chelate. Arch. Environ. Health 14: 693-697.
Schroeder, H.A., et al. 1967b. Essential trace metals in man: zinc. Relation to environmental cadmium. J. Chron. Dis. 20: 179-210.
and A. Nason. 1969. Trace metals in human hair. ---J"""".~I-nv_e_s-t. Dermatol. 59: 71-78.
45
and M. Mitchener. 1971. Toxic effects of trace element ------on the reproduction of mice and rats. Arch. Environ. Health 23: 102-106.
Shaikh, Z. and 0. Lucis. 1972a. Biological differences in cadmium and zinc turnover. Arch. Environ. Health 24: 410-425 .
. 1972b. Cadmium and zinc binding in mammalian ----=-..,,--.--~..,,.....,....--1 i ver and kidneys. Arch. Environ. Health 24: 419-425.
Sharrett, A.R. 1977. Water hardness and cardiovascular disease elements in water and human tissues. Sci. Total Environ. 7: 217-226.
Shimkin, M.B., G. Stoner and J. Theiss. 1978. Lung tumor response in mice to metals and metal salts. In Schrauzer, G.N. (Ed.) Inorganic and nutritional aspects of cancer. Plenum Press, N.Y. Pp. 85-91.
Sissoeff, I., J. Grisvard and E. Guille. 1976. Studies on metal ionsDNA interactions: specific behavior of reiterative DNA sequences. Prag. Biophys. Mol. Biol. 31: 165-199.
Smith, J.C. and E. Brown. 1976. Effects of oral contraceptive agents on trace element metabolism--a review. In Prasad, A.S. (Ed.) Trace elements in human health and disease. V II. Essential and toxic elements. Pp. 315-345.
Strain, W.H., et al. 1966. Analysis of zinc levels in hair for the diagnosis of zinc deficiency in man. J. Lab. Clin. Med. 68: 244-249.
Suzuki, K.T. and M. Yamamura. 1981. Native and induced rat kidney metallothioneins and their relation to cadmium toxicity. Arch. Environ. Contam. Toxicol. 10: 251-262.
Suzuki, S., T. Suzuki and M. Ashizawa. 1965. Proteinuria due to inhalation of cadmium stearate dust. Ind. Health 3: 73-79.
Thomas, R., J. Wilson and J. London. 1980. Multispecies retention parameters for cadmium. Environ. Res. 23: 191-207.
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Tipton, I.H. and P.L. Stewart. 1970. Patterns of elemental excretion in long-term balance studies II. Health Phys. Div. Ann. Progr. Rep. ORNL-4446: 303-314.
Travis, C.C. and A. Haddock. 1980. Interpretation of the observed age-dependency of cadmium body burdens in man. Environ. Res. 22: 46-60.
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-------· 1979. Interactions of trace elements. In Toxicity of heavy metals in the environment. Pt. 2. Marcel Dekker, N.Y. Pp. 641-668.
46
U.S. Department of Health, Education, and Welfare. 1977. Occupational diseases: a guide to their recognition. DHEW Publ. 77-181. U.S. Government Printing Office, Washington, D.C. 608pp.
~~~~~~~~~~~~~~~~~~~· 1979. Smoking and health. U.S. Government Printing Office, Washington, D.C. n.p.
Welinder, H., S. Skerfving and 0. Henriksen. 1977. Cadmium metabolism in man. Br. J. Ind. Med. 34: 221-228.
Yurachek, J., G. Clemena and W. Harrison. 1969. Analysis of human hair by spark source mass spectrometry. Anal. Chem. 37: 1666-1668.
S33IGN3ddV
1 !
Cd
Zn
APPENDIX A
PREVIOUS STUDIES ON Cd AND Zn IN HUMAN HAIR
Subjects
? Americans 66 rural Canadians 45 urban Canadians 82 U.S. males 18 Port Arthur, TX males 95 Cincinatti, OH males 47 U.S. females 21 Port Arthur, TX females 83 Cincinatti, OH females
33 Oak Ridge, Tennesseans ? Canadians
12 Egyptians 3? U.S. subjects 75 Iranian children aged 6-12 4 Egyptian males
33 Hastings, N.Z. schoolboys 33 Napier, N.Z. schoolboys 20 Iranian male students 6 New York male adults
18 U.S. male adults 82 U.S. males 64 Panamanian male adults 14 Washington, D.C. male adults c. 100 Cincinatti, OH males 18 Port Arthur, TX males 42 New Zealand males aged 18-27 16 Iranian female adults 47 U.S. females 70 Panamanian female adults c. 100 Cincinatti, OH females 21 Port Arthur, TX females 54 New Zealand females
Concentrationl (µg/g)
o. 34--1.8 i.2M(o.25--2. 7) 2.0M(0.32--3.4)
2.76 ± .483 2.2 (0.1--9.3)
2.2 ± .2 1. 77 ± .239
1.0(0.2--3.6) 2.43 ± .26
177 ± 73D 300--1000
103.3 ± 4.9 143--246
199 ± 22D 105--136
126 ± 140 132 ± 15D
181 ± 36.30 119 .6 ± 4.6
178.7(143--206) 167.o ± 5.89
142 ± 43 176 ± 370
147 156(75--454)
180 ± 25 268 ± 59.3°
172.1 ± 9.32 167 ± 1290
153 173(65--308)
19S ± 23
Analysis Technique2
SSMS PAA
II
AAS II
II
II
II
II
NAA II
AES SSMS AAS
II
NAA II
Z/D AES AAS
II
II
II
II
II
II
Z/D AAS
II
II
II
II
Reference
Yurachek et al. 1969 Chattopadhyay et al. 1977 Chattopadhyay et al. 1977 Schroeder 1969 Eads et al. 1973 Petering et al. 1973 Schroeder 1969 Eads et al. 1973 Petering et al. 1973
Bate & Dyer 1975 Perkons & Jervis 1966 Strain et al. 1966 Yurachek et al. 1969 McBean et al. 1971 Prasad et al. 1963 Bate & Dyer 1965 Bate & Dyer 1965 Reinhold et al. 1966 Strain et al. 1966 Harrison et al. 1969 Schroeder 1969 Klevay 1970 McBean et al. 1971 Petering et al. 1971 Eads et al. 1973 McKenzie 1979 Reinhold et al. 1966 Schroeder 1969 Klevay 1970 Petering et al. 1971 Eads et al. 1973 McKenzie 1979
1 Concentrations are average ± standard error unless noted (D) as standard deviation; if means were not reported medians {M) and/or ranges are given.
2 AAS = Atomic absorption spectroscopy AES = Atomic emission spectroscopy NAA = Neutron activation analysis PAA = Photon activation analysis SSMS = Spark source mass spectroscopy Z/D = Zincon/Dithizone analysis
APPENDIX B
INFORMED CONSENT
I, , hereby agree to serve
as a subject in the research project on cadmium.conducted by Neal Simonsen.
I understand that the study involves the donation of a sample of scalp
hair for trace metal analysis and candid completion or a background
questionnaire by each subject.
I understand the possible risks and discomtorts to me associated with
this study, including a demand on rrr:r time and effort involved in the filling
out or the study questionnaire as well as the' inconvenience of collecting
and tagging a sample of scalp hair.
It has been explained to me that the purpose of this study is to explore
the differences in levels of cadmium (and zinc) in the hair of individuals in
the population as they relate to smoking habits. I may not receive any direct
benefit from participating in this study, but my participation maY help to
increase knowledge which may benefit others in the future. Neal Simonsen has
offered to answer any questions I may have about the study and what is
required or me in the study •
. I understand that I am free to withdraw from participation in this study
at any time without jeopardizing 'fll:/ relationship with Portland State University.
I have read and understand the foregoing infonnation.
Date ______________________ _ Signature
---------------------------
1. Age (in years at last birthday): __ _ Weight: ---
Nwnber
Height: ----
2. Sex:
J. Race:
a Male b Female
a White (non-Hispanic) b Black c Asian or Pacific Islander d Hispanic
Country or birth: ------
e Other (please specify) -------
4. Natural predominant hair color: a Brown b Black c Blond d Red e Grey or white
s. Do you or have you smoke(d) tobacco? (Check Yes or No; i! Yes please also answer 1, ii, iii, iv and v below)
a Yes 1 Do you or did you smcike: (Check all which apply)
a Cigarettes b Cigars c A pipe
ii Are you a aurrent or only a former smoker? a Current b Former
iii How many years have you or did you smoke(d)?: iv If you are or were a cigarette smoker, how JT18.llY packs per day
do you or did you smoke, on the average?:
v If you are or were a cigarette smoker and smoke(d) one
50
brand most or the time, which brand is or was it?: -------b No
6. Do you or did you smoke marijua.~a? (Check Yes or No; it Yes please answer 1, ii and iii) a Yes
b No
i Are you a current or only a tormer smoker? a Current b Former
ii How many years have you or did you smoke(d)?s iii I! you are or were a marijuana smoker, about how many
days per month do you o~ did you smoke it, on the average?: _
7. What is the zip code ot your place or residence?:-----------
8. Are there any major refineries, smelters or other Metal or chemical industrial complexes within a mile or the place? {It Yes, please list in space provided)
a Yes:
b No c Don't know
9. If there are any other areas you regularly spend 30 hours per week or more in, please locate them by listing their zip codes:
1. ------
2. ------
J. ------10. Are there a:n:y major refineries, smelters or other indunrial complexes in these
areas? {If unsure, answer No) a Yes, in area 1. b Yes, in area 2. c Yes, in area ). d No
11. Are you regularly exposed to other people's tobacco smoke at home, work or otherwise? a Yes, for more than 5 hours per week b Yes, for 5 hours or less per week c No
12. Do you do any soldering work at home or at your job? a Yes b No
13. Are you a vegetarian? a Yes b No
14. Which of the following items are a part of your diet at least once a week, on the average? (Check all which apply)
a Fish b Anchovies c Shellfish d Oysters e Rice
15. Do you drink at least two cups of tea a week, on the average? a Yes b No
16. What hair care products do you use? (Please list)
17. How often do you wash your hair, on the average? a 4 or more times per week b 3 times or less per week
18. Do you use oral contraceptives? a Yes b No
19. Do you have any chronic conditions {such as asthma or hay fever) or current illnesses {such as the flu or strep throat)?
a Yes b No
It Yes, please list: -------------------------------------
51
4 4
4A
44
4
4 -
-·-
4 ---.-
A
4 -··
......
......
......
......
......
......
......
......
......
...-...
... ..
....... -
......
......
......
......
......
..... -
........
........
.... _.
.....
........
........
........
... _
.. ...
..,,.,
...
APPE
NDIX
C
TABL
E V
II I
HAIR
CAD
MIUM
CON
CENT
RATI
ONS
(µg/
g}
FOR
INDI
VIDU
ALS,
GROU
PED
ACCO
RDIN
G TO
Sf()
KING
HAB
ITS
Cur
rent
tob
acco
sm
oker
b
~ Fo
rmer
to
bacc
o sm
oker
c
- ~ en
cu - "' ~ LL
.
Nei
ther
cu
rren
t no
r fo
rmer
to
bacc
o sm
oker
Cur
rent
tob
acco
sm
oker
b
Form
er t
obac
co s
mok
erc
Nei
ther
cu
rren
t no
r fo
rmer
to
bacc
o sm
oker
a A
t le
ast
4 d
ays
per
mon
th
b A
t le
ast
1/3
pac
k p
er d
ay
c A
t le
ast
5 p
ack-
year
s
Not
cu
rren
t re
gu
lar
mar
ijua
na
smok
er
.751
, .5
59,
.822
.450
, .4
35 •. 5
00,
.423
, .6
80
.693
• 368
' . 4
46 '
• 444
' • 2
84 '
• 426
' 1
.27
, .6
38,
1.7
8,
.760
, .5
64,
.596
, 1
.76
, .7
96,
.524
, .5
07,
.367
, .5
92,
.573
, .4
40,
.786
, .5
73,
.432
, 1
.08
, .9
91
.800
, .5
72,
.750
, .6
57,
.960
, 1.
38
.618
, .9
58,
.621
, .7
33,
.575
.899
, .4
30,
.961
, .5
46,
.498
.t .8
10,
.384
, 1
.25
, .2
82,
. 77'
8,
.776
, .7
35,
1.4
6,
.974
, .6
53,
.886
, .9
15,
1.2
3,
.673
, .8
86,
.773
, .5
97,
.342
, .5
55,
1.7
4,
.683
, .6
06,
• 532
, .4
15,
. 599
, .4
67,
.433
, .5
59,
1.4
3,
.330
, .5
91
Cur
rent
reg
ula
r m
arij
uana
sm
oker
a
.518
, .5
88,
.594
, 1
.52
, 3.
58
Non
e
.622
, • 7
70,
.894
, 1
.02
.616
, .8
19
.423
.686
, .7
18,
.745
, .8
87
, 1.
02
~---1
APPE
NDIX
D
TABL
E IX
HAIR
ZIN
C CO
NCEN
TRAT
IONS
(µ
g/g)
FO
R IN
DIVI
DUAL
S,
GROU
PED
ACCO
RDIN
G TO
SM
OKIN
G HA
BITS
en
Cl.I
r- ~
en
Cl.I
r- ~ ~
Cur
rent
tob
acco
sm
oker
b
Form
er t
obac
co
smok
erc
Nei
ther
cur
rent
nor
fo
rmer
to
bacc
o sm
oker
Cur
rent
tob
acco
sm
oker
b
Form
er t
obac
co s
mok
erc
Nei
ther
cur
rent
nor
fo
rmer
tob
acco
sm
oker
a A
t le
ast
4 da
ys p
er m
onth
b A
t le
ast
1/3
pack
per
day
c A
t le
ast
5 pa
ck-y
ears
Not
cur
rent
reg
ular
mar
ijuan
a sm
oker
107,
13
1,
238
118,
13
0,
188,
19
6
99,
104,
12
9,
134,
13
9,
143
141,
15
6,
166,
17
4,
176,
18
0 18
0,
182,
18
5,
194,
223
, 26
9
132,
18
1,
242,
24
7,
279
158,
16
5,
175
110,
11
5,
127,
12
9,
148,
14
8 15
6,
157,
15
8,
162,
16
6,
168,
18
2, 1
84,
184,
188
, 19
0,
201,
20
3,
224,
22
8,
236,
25
2,
278,
29
1,
293'
371
Cur
rent
reg
ular
mar
ijuan
a sm
oker
a
184,
18
5,
221,
30
0
None
178,
242
, 26
9
186,
21
8
143
224,
36
8
~~--_ _.
.. I I I
APPENDIX E
SUMMARY OF SELECTED QUESTIONNAIRE RESPONSES - MAIN STUDY
Average age: 25.8 years Sex: Male 43%
Female 57%
Race: White Black Asian or Pacific Islander Hispanic
Natural predominant hair color: Brown Black Blonde Red Grey or white
Do or did smoke tobacco Do or did smoke marijuana Regularly exposed to other people's tobacco smoke:
5 or more hours per week Less than 5 hours per week Not regularly exposed
Vegetarian Eat at least once per week:
Fish Anchovies She 11 fish Oysters Rice
Drink 2+ cups tea/week Wash hair more than 3 times per week Use oral contraceptives Chronic conditions, current illness:
Hay fever or 11 allergy 11
Recent flu or cold Asthma Strep throat Ulcers Kidney infection
Males 93%
5 2
57 17 21 5
36
52
15 28 57
5
33 3
38
23
85
13 13
3
Females 96%
4
67 2
24 5 2
35
49
37 20 43
20
51
39
35
44 61
16
18 4 2
2 2